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This divergence is mechanistically important: when both receptor systems are co-stimulated in research models, somatotrophs release more GH than either pathway can produce alone, an effect attributed to the convergent activation of multiple second-messenger systems on the same secretory cell.[1][2] The PLC pathway also engages diacylglycerol/PKC signaling that contributes to GH gene transcription via CREB phosphorylation, supporting sustained somatotroph output during repeat dosing.[7] Outside the pituitary, ipamorelin engages GHS-R1a expressed on enteric cholinergic neurons, where it activates atropine- and tetrodotoxin-sensitive excitatory pathways that accelerate gastric and colonic transit — the mechanistic basis for its evaluation in postoperative ileus models.[4][5] The compound also binds peripheral ghrelin receptors on enteric afferent neurons, attenuating visceromotor responses to noxious distension in rat models — an effect blocked by selective ghrelin receptor antagonists, confirming receptor specificity.[17] vs

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